Hypertension in Pregnancy
Tony Nicoll
Consultant Obstetrician
Ninewells Hospital
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Outline
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Objectives
Physiology
Classification
Pre-eclampsia
Pathogenesis
Management
Eclampsia
Conclusions
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Objectives
• Understand the processes involved in antenatal
care, surveillance in pregnancy, and the roles of
the professionals involved (Outcomes 1-11)
• Demonstrate a knowledge of the common
problems encountered in obstetric practice
(Outcomes 3,4,5,8)
Hypertension in Pregnancy
• Hypertension affects 10-15% of all pregnancies
• Mild pre-eclampsia affects 10% of primigravid women
• Severe pre-eclampsia affects 1% of primigravid women
• Eclampsia affects 1/2000 pregnancies
• Death from eclampsia = 2%
• Pre-eclampsia is the commonest cause of iatrogenic
prematurity
• Up to 25% of antenatal admissions are due to hypertension
Blood Pressure in Pregnancy
• Blood pressure (BP) proportional to systemic
vascular resistance and cardiac output
• Pregnancy  Vasodilatation
• BP falls in early pregnancy
• Nadir reached at 22-24 weeks
• Steady rise until Term
• BP falls after delivery but subsequently rises and
peaks at day 3-4 P/N
Hypertension
• ≥140/90 mmHg on 2 occasions
• DBP >110 mmHg
• ACOG - >30/15 mmHg compared to booking BP
Hypertension in Pregnancy
• Pre-existing hypertension
• Pregnancy Induced Hypertension (PIH)
• Pre-eclampsia
Pre-existing Hypertension
• Diagnosis prior to pregnancy
• Likely if hypertension in early pregnancy
(PET / PIH diseases of second half of pregnancy)
• May be retrospective diagnosis if BP has not
returned to normal within 3 months of delivery
• Consider secondary causes - renal / cardiac,
Cushing’s, Conn’s, Phaeochromocytoma
• Risks include PET (X2), IUGR and abruption
PIH
• Second half of pregnancy
• Resolves within 6/52 of delivery
• No proteinuria or other features of pre-eclampsia
• Better outcomes than pre-eclampsia
• 15% progression to pre-eclampsia - depends on
gestation
• Rate of recurrence is high
Pre-eclampsia
Pre-eclampsia
• Hypertension
• Proteinuria (≥0.3g/l or ≥0.3g/24h)
• Oedema
• Absence does not exclude the diagnosis
Pre-eclampsia
• A pregnancy-specific multi-system disorder with
unpredictable, variable and widespread
manifestations
• May be asymptomatic at time of first presentation
• Diffuse vascular endothelial dysfunction widespread
circulatory disturbance
• Renal / Hepatic / Cardiovascular / Haematology /
CNS / Placenta
Pathogenesis
• Genetic predisposition
• Stage 1 - abnormal placental perfusion
• Stage 2 - maternal syndrome
Pathogenesis
• Abnormal placentation and trophoblast invasion  failure
of normal vascular remodelling
• Spiral arteries fail to adapt to become high capacitance,
low resistance vessels
• Placental ischaemia  widespread endothelial damage
and dysfunction
• Mechanism unclear (??oxidative stress / PGI2 : TXA2
imbalance / NO)
• Endothelial Activation 
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 Capillary Permeability
 Expression of CAM
 Prothrombotic Factors
 Platelet aggregration
Vasoconstriction
NonPregnant
Preeclampsia
Normal
Placentation
A Multi-system Disorder
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CNS
Renal
Hepatic
Haematological
Pulmonary
Cardiovascular
Placental
CNS Disease
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Eclampsia
Hypertensive encephalopathy
Intracranial haemorrhage
Cerebral Oedema
Cortical Blindness
Cranial Nerve Palsy
Renal disease
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 GFR
Proteinuria
 serum uric acid (also placental ischaemia)
 creatinine / potassium / urea
Oliguria /anuria
Acute renal failure
• acute tubular necrosis
• renal cortical necrosis
Liver Disease
• Epigastric/ RUQ pain
• Abnormal liver enzymes
• Hepatic capsule rupture
• HELLP Syndrome
Haemolysis, Elevated Liver Enzymes,
Low Platelets
• high morbidity/ mortality
Haematological Disease
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 Plasma Volume
Haemo-concentration
Thrombocytopenia
Haemolysis
Disseminated Intravascular Coagulation
Cardiac / Pulmonary
Disease
• Pulmonary oedema  ARDS
• iatrogenic
• disorder related
• Pulmonary Embolus
• High mortality
Placental Disease
• Intrauterine growth restriction (IUGR)
• Placental Abruption
• Intrauterine Death
Symptoms
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Headache
Visual disturbance
Epigastric / RUQ pain
Nausea / vomiting
Rapidly progressive oedema
• Considerable variation in timing, progression and
order of symptoms
Signs
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Hypertension
Proteinuria
Oedema
Abdominal tenderness
Disorientation
SGA
IUD
Hyper-reflexia / involuntary movements / clonus
Investigations
• Urea & Electrolytes
• Serum Urate
• Liver Function Tests
• Full Blood Count
• Coagulation Screen
• CTG
• Ultrasound - biometry, AFI, Doppler
Management
• Assess risk at booking
• Hypertension < 20 weeks - look for secondary
cause
• Antenatal screening - BP, urine, MUAD
• Treat hypertension
• Maternal & fetal surveillance
• Timing of Delivery
• PIH can be managed as O/P in Day Care Unit
Risk Factors
• Maternal Age (>40 years 2X)
• Maternal BMI (>30 2X)
• Family History (20-25% if mother affected, up to
40% if sister)
• Parity (first pregnancy 2-3X)
• Multiple pregnancy (Twins 2X)
• Previous PET (7X)
• Molar Pregnancy / Triploidy
• Multiparous
disease
women
develop
more
severe
Medical Risk Factors
• Pre-existing renal disease
• Pre-existing hypertension
• Diabetes Mellitus
• Connective Tissue Disease
• Thrombophilias (congenital / acquired)
Predicting Pre-eclampsia
Normal MUAD
Notch
Maternal Uterine Artery Doppler
20 - 24 weeks
Antenatal Screening
• When to refer to AN DCU?
BP  140/90
(++) proteinuria
  oedema
symptoms - esp persistent headache
• For every 1000 “Low-risk” patients:
100 hypertensive
60 normal - 20 will return
20 DCU follow up - 10 admitted
20 admitted
When to admit?
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BP >170/110 OR >140/90 with (++) proteinuria
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Significant symptoms - headache / visual disturbance /
abdominal pain
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Abnormal biochemistry
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Significant proteinuria - >300mg / 24h
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Need for antihypertensive therapy
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Signs of fetal compromise
Inpatient Assessment
• Blood Pressure - 4 hourly
• Urinalysis - daily
• Input / output fluid balance chart
• 24 hour urine collection - if proteinuria on urinalysis
• Bloods - FBC, U&Es, Urate, LFTs. Minimum X2 per week
Fetal Surveillance
• Fetal Movements
Normal
• CTG - daily
AEDF
• Ultrasound
Biometry
Amniotic Fluid Index
Umbilical Artery Doppler
REDF
Treatment of Hypertension
• Treat regardless of aetiology
• With MAP ≥150 mmHg there is significant risk of cerebral
haemorrhage
• Most treat if BP ≥150/100 mmHg
• BP ≥ 170/110 mmHg requires immediate Rx
• Aim for 140-150/90-100 mmHg
• Control of blood pressure does not reduce the risk of
developing pre-eclampsia
Treatment of Hypertension
Mode of
Action
Starting
Dose
Maximum
Dose
Contraindications
Breast
Feeding
Methyl
Dopa
Centrally
acting 
agonist
250mg bd
1 gram tds
Depression
Yes
Labetolol
+
antagonist
100mg bd
600mg qid
Asthma
Yes
Nifedipine
SR
Ca channel
antagonist
10mg bd
40mg bd
Yes
Hydralazine
Vasodilator
25mg tds
75mg qid
Yes
(Avoid Diuretics / ACE Inhibitors)
When to Deliver?
• The only cure for pre-eclampsia is delivery
• Mother must be stablised before delivery
• Consider expectant management if pre-term
• Most women delivered within 2 weeks of
diagnosis
Indications for Delivery
• Term gestation
• Inability to control BP
• Rapidly deteriorating biochemistry / haematology
• Eclampsia
• Other Crisis
• Fetal Compromise - REDF, abnormal CTG
Crises in Pre-eclampsia
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Eclampsia
HELLP syndrome
Pulmonary Oedema
Placental Abruption
Cerebral Haemorrhage
Cortical Blindness
DIC
Acute Renal Failure
Hepatic Rupture
Steroids
• Promote fetal lung surfactant production
• ↓ neonatal respiratory distress syndrome (RDS)
by up to 50% if administered 24-48h before
delivery
• Administer up to 36 weeks
• Only significant effects up to 34 weeks. Proven
benefit up to 1 week
• Betamethasone preferred to Dexamethasone
• 1 course = 12mg Betamethasone IM X2 injections
24 hours apart
Eclampsia
Eclampsia
• Tonic-clonic (grand mal) seizure occuring with
features of pre-eclampsia
• >1/3 will have seizure before onset of
hypertension / proteinuria
• Ante-partum (38%) / Intra-partum (16%) / postpartum (44%)
• More common in teenagers
• Associated with ischaemia / vasospasm
Management of Severe PET /
Eclampsia
• Control BP
• Stop / Prevent Seizures
• Fluid Balance
• Delivery
Antihypertensives
• IV Labetolol
• IV Hydralazine
• Beware hypotension – fetoplacental unit
Seizure Treatment / Prophylaxis
MAGNESIUM SULPHATE
Loading dose:
4g IV over 5 minutes
Maintenance dose:
IV infusion 1g/h
If further seizures administer 2g Mg SO4
If persistent seizures consider diazepam 10mg IV
Fluid Balance
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Main cause of death = pulmonary oedema
(Capillary leak / fluid overload / cardiac failure)
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Oliguria in 30%. Does not require intervention
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Any doubts about renal function  urine osmolality
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Fluid challenges are potentially dangerous
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Safer to run a patient “dry” - 80 ml/h
Labour and Delivery
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Aim for vaginal delivery if possible
Control BP
Epidural anaesthesia
Continuous electronic fetal monitoring
Avoid ergometrine
Caution with iv fluids
Postpartum Management
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Breast feeding
Contraception
BP management
Counselling
Future risk
– Depends on other medical factors
– Gestation dependent (28/40 - 40%, 32/40 - 30%)
• Long term CVD risk
Low Dose Aspirin
• Aspirin - inhibits cyclo-oxygenase  prevents TXA2
synthesis
• 75mg Aspirin 15%  reduction in PET (NNT=90)
• May be more beneficial in preventing severe early onset
pre-eclampsia (MRC CLASP Trial)
• Safe
• Used for high risk women - Renal, DM, APS, Multiple risk
factors, previous PET
• Commence before 12 weeks
NICE Aug 2010
Calcium, Antioxidants
& Folic Acid
• Calcium supplementation (>1gram / day) may reduce
risk of hypertension (30%), PET (52%) and maternal
death (20%). Did not affect pre-term birth or stillbirth
(Hofmeyr et al Cochrane Database 2006)
• Antioxidants not effective (Poston et al.
VIP Study, Lancet 2006)
• Mid trimester folic acid also appears to be effective in
preventing pre-eclampsia (73% reduction) (Wen et al AJOG
2008)
Conclusions
• Hypertension in pregnancy is common
• Pre-eclampsia is a multi-system disorder
unpredictable and variable manifestations
with
• Pathogenesis involves abnormal placentation and
widespread endothelial dysfunction
• Supportive management requires maternal and fetal
surveillance
• No cure other than delivery
• Maternal risks balanced against risks of prematurity